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154
Manipal Manual of Surgery
Anal warts, diarrhoea
Perianal sepsis—abscesses
Anal ulceration, fissures
Reduced sphincter tone and anal incontinence
in homosexuals
II. Abdominal pain: This is due to a gastrointestinal
opportunistic infection, usually caused by cyto­megalovirus (CMV). It is a type of colitis and produces abdominal pain, cramps, loose stools, and blood and mucus in the stools, resulting in emaciation. Flexible sigmoidoscopy may reveal severe proctitis. Severe colitis may lead to acute toxic dilatation of the colon.
Biliary tract infection by cryptosporidium may
cause acute cholecystitis. AIDS-related sclerosing cholangitis may occur, resulting in right upper quadrant pain.
Abdominal lymphoma with involvement of the
liver and spleen may also cause abdominal pain.
Severe abdominal pain may be due to perfora-
tion of the small or large bowel and should be treated as an emergency.
Appendicitis is also common due to CMV
infection.
III. Lymphoma, Kaposi’s sarcoma, etc. They occur due
to reduced cellular immunity because of:
Immunosuppression used in organ transplantation
Severe malnourishment
HIV infection
Lymphoproliferative disease (Key Box 25.5)
Kaposi’s sarcoma may affect the skin surface,
gastrointestinal tract, lungs, etc. It presents as pigmented multifocal skin lesions.
Key Box 25.5
HIV-associated Lymphomas
1. Lymphomas in HIV patients—‘B’ symptoms and intra­abdominal and extranodal involvement including lung, bone marrow and liver are common.
2. HIV-associated lymphomas are Diffuse Large Cell (DLC) or Burkitt’s lymphoma.
3. HIV-associated lymphomas present as ascites/pleural effusion, etc.
4. Treatment should be HAART (highly active anti­retroviral therapy) with standard chemotherapy and granulocyte-colony stimulating factor.
IV. Oesophageal ulcers may present as dysphagia and
odynophagia. Endoscopy should be done using a glove and the scope should be washed thoroughly with soap and water and immersed in cetrimide solution for 15 minutes.
V. Lymphadenopathy: Very often, surgeons are called
for lymph node biopsy to evaluate fever or genera­lised lymphadenopathy. All universal precautions must be observed in all patients.
A 23-year-old lady, carrying a 6-month-old child, presented to us with severe dysphagia and odynophagia. Endoscopy revealed extensive, unusual, oesophageal ulcers which prompted us to conduct a HIV test. It was positive. We called her husband and wanted to convey the message to him, but before we could, he said, ‘I am HIV-positive, my wife is HIV-positive, and even my child is HIV-positive!!!’
Risk of HIV Transmission
Risk of HIV transmission from patient to surgeon is
very low but dangerous.
Routine use of barriers (gloves and goggles), washing
hands before and after examination of the patient, and careful handling of sharps and needles greatly reduce transmission of the disease.
Post-exposure prophylaxis should begin immediately.
Routes of exposure and incidence of HIV transmission:
Percutaneous—0.3%
– – Cutaneous— 0.09% – Mucus membrane—0.09%.
Post-Exposure Prophylaxis (Occupational Exposure)
1. Immediate decontamination of the injured area— washing the area with soap and water for cutaneous and percutaneous exposure. For punctured wounds, clean with alcohol-based agents. For infected eyes, irrigate with a copious amount of sterile water or saline.
. Early reporting of exposure: Blood tests have to be
2
done.
3. As soon as possible or within 2 hours, post-exposure prophylaxis should be done using the 3-drug regimen given below.
Raltegravir 400 mg 3 times/day, tenofovir 300 mg/ day and emtricitabine 200 mg/day.
Section II General Surgery
Chronic Infectious Disease
155
1. Which of the following statements about actino­mycosis is false?
A. Sulphur granules are gram-positive mycelia
surrounded by gram-positive clubs
B. Actinomyces israelii is an anaerobic organism
. The organism has both bacterial and fungal
C
characteristics
D. Multiple subcutaneous nodules over the jaw are
characteristic
2. The following are true for treatment of actinomycosis except:
A. Crystalline penicillin is the drug of choice
. Tetracyclines have no role in the treatment
B C. Surgery may be required for abdominal actino-
mycosis
D. Ceftriaxone may be used for pulmonary
actinomycosis
3. The following are features of tuberculoid leprosy except:
A. Bacilli are a few
. Hypopigmented skin patches are seen
B C. Nerve thickening is often a finding D. Face and nose involvement is diagnostic of the
condition
4. Hutchinson’s triad does not include which of the following?
A. Interstitial keratitis
. 8th nerve deafness
B C. Chancre D. Narrow-edged wide-spaced permanent incisors
5. Gummatous ulcer has all the following features except:
A. Commonly seen in the subcutaneous tissues B
. Floor has wash leather slough
C. Healing results in a hypertrophic scar D. It has punched out edges
6. The following are features of secondary syphilis except:
A. Vesicles all over the body
. Coppery red rashes
B C. Snail track ulcers D. Epitrochlear node enlargement
7. The characteristic feature of primary genital chancre in syphilis is:
A. It occurs 48 hours after sexual exposure
. Multiple ulcers
B C. Indurated ulcer with large, rubbery, inguinal nodes D. Indurated, single, painless ulcer
8. The following are features of Treponema pallidum except:
A. It is a spirochaete B
. It is a gram-negative organism C. It is visible by dark field illumination D. It does not have a helical structure
9. The following are true for cytomegalovirus (CMV) infections, except:
A. It causes abdominal pain and colitis
. It is related to chickenpox–herpesvirus
B C. It may be transmitted by blood transfusion and
organ transplantation
D. It is not transmitted to the child during pregnancy
10. The following may be HIV-associated lymphomas except:
A. B cell lymphoma
. Diffuse large cell lymphoma
B C. Burkitt’s lymphoma D. Hodgkin’s lymphoma
Answers
1. A 2. B 3. D 4. C 5. C 6. A 7. D 8. D 9. D 10. D
Section II General Surgery
26
Differential Diagnosis of
Leg Ulcer and Pressure Sore
Clinical examination of an ulcerManagementWound dressingsTraumatic ulcerVenous ulcerTrophic ulcerTropical ulcer
INTRODUCTION
Leg ulcers are one of the important topics in surgery. They occur in children, adults, and the elderly. No age or sex is spared. Varying aetiological factors and the presence of complicated systemic diseases make the treatment of ulcers very difficult. Chronic ulcers in the elderly definitely cause considerable morbidity, and diabetic ulcer of the leg may cause life-threatening complications such as diabetic ketoacidosis and septicaemia. Hence, it is necessary to do a careful clinical examination of the ulcer to arrive at the diagnosis and plan the appropriate treatment.
Definition
An ulcer is a discontinuity of the skin or mucous membrane which occurs due to microscopic death of the tissues. Thus, ulcers may occur anywhere in the body (skin), oral cavity, penis (mucous membrane), duodenum, intestine, etc. In this chapter, lower limb ulcers will be discussed.
Classification
Ulcers may be classified based on the pathology or clinical features.
I. Pathological Classification (Key Box 26.1)
A. Nonspecific ulcers
1. Traumatic: This is the most common cause of leg
ulcers. Trauma may be mechanical, physical due to burns or radiation, or chemical due to acids.
Post-thrombotic ulcerRare ulcersDiabetic ulcer footAmit Jain’s classification for diabetic footVACPressure soreMaggot therapy
2. Venous ulcers: They include varicose ulcers and post-
thrombotic ulcers, which may occur following deep vein thrombosis.
3. Arterial ulcers: Following are a few examples of
arterial ulcers:
Buerger’s disease—common
Atherosclerotic vascular disease—common
Vasospastic disorders such as Raynaud’s disease—
uncommon
Martorell’s ulcers or hypertensive ulcers—rare
Patients with rheumatoid arthritis may develop leg
or foot ulcers due to vasculitis.
. Neurogenic ulcer (neuropathic ulcer, trophic ulcers)
4
Leprosy and diabetes are the common causes
Paraplegia, meningomyelocoele, posterior tibial
nerve injury, and tabes dorsalis are other causes.
Key Box 26.1
Pathological Classification of Ulcer
A. Nonspecific ulcers
1. Traumatic 2. Venous
3. Arterial 4. Neurogenic—trophic
5. Tropical 6. Diabetic
7. Blood dyscrasias
B. Specific ulcers C. Malignant ulcers
156
Differential Diagnosis of Leg Ulcer and Pressure Sore
5. Tropical ulcer: It is a rare ulcer due to malnutrition associated with infection caused by Vincent’s organisms—Borrelia vincentii and Fusiforme organisms.
6. Diabetic foot ulcer or diabetic leg ulcer.
7. Blood dyscrasias: Sickle cell anaemia, thalassaemia,
leukaemia, etc. may produce recurrent ulcerations over the leg.
157
B. Specific ulcers
These are due to a specific type of organism (e.g. tubercular ulcer, syphilitic ulcer, actinomycotic ulcer).
C. Malignant ulcers
These are squamous cell carcinoma, basal cell carci­noma, and malignant melanoma. Malignant ulcers are discussed in Chapter 31.
II. Clinical Classification (Table 26.1)
CLINICAL EXAMINATION OF AN ULCER
Inspection
1. Location of the ulcer
1
Arterial ulcer: Tip of the toes,
dorsum of the foot.
Long saphenous varicosity with ulcer: Medial side
of the leg.
Short saphenous varicosity with ulcer: Lateral side
of the leg just above the lateral malleolus.
Perforating ulcers: Over the sole at pressure points.
Nonhealing ulcer: Over the shin and lateral
malleolus.
2. Floor of the ulcer: This is the part of the ulcer which
is exposed or seen.
Red granulation tissue: Healing ulcer (Fig. 26.1)
Necrotic tissue and slough: Spreading ulcer (Fig. 26.2)
2
Pale, scanty granulation tissue: Tubercular
ulcer
Wash-leather slough: Gummatous ulcer
Fig. 26.1: Traumatic
ulcer with red granulation tissue in the floor—typical healing ulcer
Fig. 26.2: Slough—dead soft tissue—
typical spreading ulcer in a diabetic patient
Part of the bone: Neuropathic ulcer
Nodular: Epithelioma
Black tissue: Malignant melanoma
3. Discharge from the ulcer
Serous: Healing ulcer
Purulent: Spreading ulcer
Bloody: Malignant ulcer
Discharge with bony spicules: Osteomyelitis
Greenish: Pseudomonas infection
4. Edge: This is between the floor and the margin of the
ulcer. The margin is the junction between the normal
epithelium and the ulcer. It represents the area of maximum cellular activity. If destruction dominates,
as in spreading ulcers, the edge is inflamed, oede­matous and angry-looking (stage of extension). When an ulcer shows evidence of healing, the edge will be bluish due to granulation tissue covered by thin epithelium (stage of transition). In a healed ulcer, the outermost part of the edge is whitish due to fibrosis (stage of repair).
The types of ulcer edges are presented in Fig. 26.3.
Sloping edge is seen in all healing ulcers such as
traumatic ulcers and venous ulcers (Fig. 26.4).
Table 26.1 Clinical classification
A. Spreading B. Callus C. Healing
No granulation tissue Pale granulation tissue Red granulation tissue
Plenty of discharge Serous discharge Minimal serous discharge
Excessive slough Slough present Slough absent
Surrounding area inflamed and Induration at the base, edge and Signs of inflammation are minimal
oedematous surrounding area
Purulent smell present Smell can be present Smell is absent
1
When there is a block in the pipelines supplying water, distal houses suffer the maximum. Is it not?
2
It is described as apple jelly granulation tissue.
Section II General Surgery
158
Manipal Manual of Surgery
Punched out edge is seen in gummatous ulcers
and trophic ulcers. Gummatous ulcers have punched out edges due to endarteritis obliterans caused by syphilitic organisms. Chronic, non­healing ulcers may also have punched out edges (Fig. 26.5).
Undermined edge is seen in tubercular ulcers,
probably due to more destruction of the sub­cutaneous tissues than the skin. The edge is classically thin and bluish in colour (Fig. 26.6).
Raised (beaded) edge is seen in rodent ulcers or
basal cell carcinoma (Fig. 26.7).
Everted (rolled out) edge is diagnostic of
squamous cell carcinoma (Fig. 26.8). The edge grows very rapidly and occupies the normal skin and, thus, becomes everted.
5. Surrounding area
Thick and pigmented: Varicose ulcer.
Thin and dark: Arterial ulcer.
Red and oedematous: Spreading ulcers like
diabetic ulcer.
Scar around the ulcer: Marjolin’s ulcer.
Palpation
. Edge: Induration (hardness) of the edge is charac-
1
teristic of squamous cell carcinoma. Some degree of induration may also be seen in chronic ulcers and
long-standing varicose ulcers. Induration occurs due to extensive fibrosis. It is said to be a host defense mechanism. Because of fibrosis, lymphatic spread is delayed. Tenderness of the edge is characteristic of infected ulcers and arterial ulcers.
2. Base: It is the area on which the ulcer rests. Pick up the
ulcer between the thumb and index finger to appreciate the tissues underneath. If the ulcer cannot be lifted up, the base cannot be made out. The base may be tendon, muscle, or bone, depending on the site of ulcer. Marked induration at the base is diagnostic of squamous cell carcinoma. Hunterian chancre is a benign ulcer and produces significant induration. Hence, it is also known as hard chancre (Key Box 26.2).
Key Box 26.2
Induration
It means hardnessMaximum induration: Squamous cell carcinomaMinimal induration: Malignant melanomaBrawny induration: AbscessCyanotic induration: Chronic venous congestion as in
varicose ulcer
The base and the surrounding area should be examined
for induration
Fig. 26.3: Different types of edges of ulcer
Fig. 26.6: Undermined edge—tubercular
sinus/ulcer
Section II General Surgery
Fig. 26.4: Sloping edge
Fig. 26.7: Raised edge—basal cell carci-
noma (Courtesy: Prof Vidyadhar Kinhal, Head, Surgery, VIMS, Bellary, Karnataka)
Fig. 26.5: Punched out edge—neuropathic
ulcer (classically described for gummatous ulcer)
Fig. 26.8: Everted edge—squamous cell
carcinoma
Differential Diagnosis of Leg Ulcer and Pressure Sore
159
3. Mobility: A gentle attempt is made to move the ulcer
to know its fixity to the underlying tissues. Malignant ulcers are usually fixed, whereas benign ulcers are not.
4. Bleeding: A malignant ulcer is friable, like a cauli-
flower. On gentle palpation, it bleeds. Granulation tissue, as present in a healing ulcer, also bleeds.
1
5. Surrounding area: Thickening and induration is
found in squamous cell carcinoma. Tenderness and pitting on pressure indicates spreading inflammation surrounding the ulcer.
Relevant Clinical Examination
. Regional lymph nodes
1
Tender and enlarged: Acute secondary infection
Nontender and enlarged: Chronic infection
Nontender and hard: Squamous cell carcinoma
Nontender, large, firm, multiple: Malignant
melanoma.
2. Peripheral vessels: Detailed examination of peri-
pheral vessels is discussed under peripheral vascular disease. However, the dorsalis pedis, posterior tibial, popliteal, and femoral arteries should be palpated in cases of lower limb ulcers. Presence of weak pulses or absent pulses indicates peripheral vascular disease.
3. Sensations: Loss of vibration sense and loss of ankle
jerk occur early in cases of diabetic neuropathy. Later, touch and pain are lost. Totally anaesthetic feet are
characteristic of leprosy.
4. Function of the joint: Movements of the involved joint
are restricted either due to pain, involvement of the joint, or infiltration into the joint by malignant ulcers.
5. Varicose veins: If present, it is most probably a
varicose ulcer. However, A-V fistulas may present as distal ulcers, with arterialisation of veins and a continuous murmur.
Systemic Examination
Central nervous system (CNS) and spine in neuro-
pathic ulcers. There may be gibbus, as in cases of TB spine, or an operated scar due to myelomeningocele, etc. See clinical notes.
An 18-year-old girl with a nonhealing trophic ulcer was examined by a postgraduate student. He gave a diagnosis of trophic (neuropathic) ulcer due to leprosy as first diag­nosis followed by polyneuropathy. He failed. It was a case of myelomeningocoele. The candidate had not examined the spine! The patient had an operated myelomeningocele.
Splenomegaly in blood dyscrasias, such as in early
stages of sickle cell anaemia.
Cardiovascular system (CVS) may reveal a murmur,
as in cases of arteriovenous fistula or features suggestive of cardiac diseases.
A summary of the clinical examination of an ulcer is
given in Key Box 26.3.
Key Box 26.3
Clinical Examination of an Ulcer
Inspection
Location, size, shape, floor, edge, discharge, surrounding
area
Palpation
Tenderness, local rise of temperature, bleeding on
touch, consistency of the ulcer, edge, surrounding area—oedema, mobility
Regional lymph nodesSensationsPulsationsFunction of the jointSystemic examination
Investigations
1. Complete blood picture: Hb%, TC, DC, ESR,
peripheral smear.
Low Hb% is found in a chronic ulcer. It may be
nutritional or due to frequent blood loss during dressings as in a diabetic ulcer.
High total count indicates infection.
Peripheral smear is done to rule out anaemia and
sickle cell disease.
2. Blood sugar estimation: Both fasting and post-
prandial.
3. Chest X-ray: Many of these patients are smokers.
They may have restricted pulmonary diseases.
4. Pus for culture/sensitivity.
5. Doppler/duplex scan/lower limb angiography in
cases of arterial diseases and venous diseases. More details are given in the respective chapters.
6. X-ray of the part: It is done in look for osteomyelitis—
common in diabetic ulcers.
7. MRI foot may be required to know the extent of the
disease as in spreading ulcers or in chronic ulcers due to diabetes (rocker bottom foot) or due to Madura mycosis. In these type of cases, saving of foot becomes difficult. Amputation may be required.
8. Biopsy: Nonhealing/malignant ulcers.
1
Granulation tissue is made up of capillaries and fibroblasts. Hence, it gives rise to fresh blood loss.
Section II General Surgery
160
Manipal Manual of Surgery
Treatment of Ulcers
It may be discussed under the following headings:
. Treatment of spreading ulcers
1
2. Treatment of healing ulcers
3. Treatment of chronic ulcers
4. Treatment of the underlying disease
1. Treatment of Spreading Ulcers
After obtaining pus culture/sensitivity report,
appropriate antibiotics are given. Many solutions are available to treat the slough, such as hydrogen peroxide and EUSol.
1
Hydrogen peroxide (diluted), when poured over the
wound, liberates nascent oxygen which bubbles out and helps in separating the slough. EUSol also
Table 26.2 Management classes of wound dressings, debridement agents and skin replacements currently available
Class
1. Debriding agents
Hydrogen peroxide
EUSol
1
Composition
releases nascent
H
2O2
oxygen which bubbles out and slough comes to surface. Hypochlorite solution
Characters/Functions
Destroys anaerobic bacteria; heat generated causes vasoconstriction and haemostasis, frothing brings debris to the surface Mild debriding action
separates the slough. Because there are reports that
and EUSol may cause more damage, they are
H
2O2
no longer used.
Partially separated slough needs to be removed daily
or on alternate days.
Excessive granulation tissue or pouting granulation
tissue (proud flesh) needs to be decapitated by excision or by the application of copper sulphate or silver nitrate solution.
By repeated dressings, the slough separates and the
discharge minimizes, resulting in a healing ulcer with healthy red granulation tissue. Management thereafter is like that of a healing ulcer.
Table 26.2 presents the various ulcer dressings that
are available today.
Commercial examples/ comments
Both these are not favoured today (EUSol is Edinburgh University
Solution)
2. Polymeric films
3. Hydrocolloid dressings
4.Alginates
5.Miscellaneous
Gauze
Tulles
6. Medicated
dressings
Impregnated
gauzes
7. Platelet-derived
growth factor (PDGF)
8. Endothelial-
derived growth factor (EDGF)
Plastic (polyurethane); semipermeable Hydrophilic colloidal particles and adhesive. It is impermeable to fluids and bacteria
Polymer gel contains mannuronic acid and glucuronic acid—seaweed polymer that forms a gel when it absorbs fluid
Woven cotton fibres
Medications
Fine mesh fabric (silicone, nylon) with dermal porcine collagens
Acts through tyrosine
kinase receptor
Allows water vapour permeation; adhesive
Absorbs fluid; necrotic tissue autolysis; little adherence; occlusive forms complex structures with water and aids in atraumatic removal of the dressing, hydrocol allows a high rate of evaporation without compromising wound hydration
Absorbs exudates; nonadherent, nonirritating, requires a cover dressing (permeable)
Along with silver, antimicrobial action against MRSA and pseudomonas.
Permeable with desiccation; debridement; painful removal
Increased epithelialisation by 25–30%
Nonadherent; semipermeable
Stimulates growth of cells and angiogenesis; increases granulation tissue; stimulation of repair—used when blood supply is good, classically neuropathic nonhealing ulcers of diabetics
Opsite; Tegaderm
Duoderm, Intrasite
Algisorb, Sorbsan should not be used in presence of hepatic or renal impairment
Zinc oxide, Neomycin, Bacitracin, Zinc
Biobrane II
Plemin, Regen-D
Costly
1
Section II General Surgery
EUSol—Edinburgh University Solution (hypochlorite solution).
Differential Diagnosis of Leg Ulcer and Pressure Sore
161
2. Treatment of Healing Ulcers
Regular dressings for a few days with antiseptic creams
(liquid iodine, zinc oxide, silver sulphadiazine, etc.).
Swab to rule out the presence of Streptococcus haemo-
lyticus, which is a contraindication for skin grafting.
If the ulcer is small, it heals on its own by epithelialisa-
tion from the cut edge.
If the ulcer is large, a free split skin graft is applied as
early as possible (Key Box 26.4).
Key Box 26.4
Advantages of Split Skin Graft
Wound healing occurs fastSecondary infection is avoided because of early skin
cover
It prevents contracturesIt prevents Marjolin’s ulcer—squamous cell carcinoma
arising from scar tissues
3. Treatment of Chronic Ulcers
These are the ulcers which do not respond to conven­tional methods of treatment. Some special forms of treatment are available, but their efficacy is doubtful.
Infrared radiation, short-wave therapy, and ultra-
violet rays decrease the size of the ulcer.
Amnion helps in epithelialisation.
Chorion helps in the formation of granulation tissue
(Fig. 26.9). These ulcers may ultimately require skin grafting.
TRAUMATIC ULCER (Fig. 26.10)
It may occur anywhere over the body. However, it is more common in areas where the skin is close to bony prominences (e.g. shin, malleoli), over which there are no muscles. They are usually single, very painful ulcers of healing type. With proper dressings and antibiotics, they usually heal within 5–7 days.
Footballer’s ulcer refers to a nonhealing ulcer over
the shin due to direct trauma caused by a football. Sometimes, these ulcers may take a long time to heal. If not treated properly, they may become adherent to the bone.
VENOUS ULCER (Fig. 26.11)
Occurs due to increased venous hydrostatic pressure
Usually associated with varicose veins
Located on the medial side of lower one-third of the
leg in cases of long saphenous varicosity and on the lateral aspect of the leg in cases of short saphenous varicosity
Shallow and superficial
Never penetrates the deep fascia
Usually painless, unless it is infected or causes
periostitis tibia
Shows evidence of healing
Typically surrounded by pigmented skin
ARTERIAL/ISCHAEMIC ULCER (Fig. 26.12)
Fig. 26.9: Five days of usage of epidermal growth factor—
granulation tissue started growing
4. Treatment of the Underlying Disease (vide infra)
Differential Diagnosis of Ulcers (Table 26.3)
Table 26.3 Causes of ulcer
Common causes Uncommon causes Rare causes
Varicose ulcer Neurogenic ulcer Martorell’s ulcer
Arterial ulcer Tropical ulcer Bazin’s disease
Diabetic ulcer Post-thrombotic ulcer
Malignant skin ulcer
It is very painful and occurs in young patients with Buerger’s disease or in elderly patients with athero­sclerotic vascular disease. It commonly occurs on the tips of toes and fingers (Fig. 26.13). The ulcer is dry, deep,
Fig. 26.10: Traumatic multiple
ulcers over the skin—classical site
Fig. 26.11: Varicose ulcer—
pigmentation is characteristic
Section II General Surgery
162
Table 26.4 Differences between arterial and venous ulcers
Arterial ulcer Venous ulcer
Location Tips of toes Medial or lateral side of leg Pain Very painful Absent Number and shape Many and irregular Single and oval Depth Deep, penetrates deep fascia Superficial, does not penetrate deep fascia Pigmentation Not a feature Usually present Nature of the vessels Peripheral pulses are weak or absent; Peripheral pulses are normal; veins are dilated
veins are not dilated
Manipal Manual of Surgery
– Alcoholic neuropathy – Nerve injuries – Transverse myelitis
Trophic ulcers are caused by inadequate blood
supply, malnutrition, and neurological deficits.
The ulcer develops over pressure points such as
beneath the heel, beneath the first and fifth meta­tarsals, and the gluteal region (decubitus ulcer). It develops as a callosity, gets infected, suppurates, and leaves a central hole that discharges pus. Slowly, it burrows deep inside and may involve the bone and
Fig. 26.12: Ischaemic
ulcer on the dorsum of the foot—typical site
Fig. 26.13: Polycythaemia causing
gangrene of toes
cause osteomyelitis. Hence, it is also known as a perforating ulcer. End stage is Charcot’s foot syndrome with varying degrees of bone and joint destruction and disorganization secondary to
and penetrates the deep fascia. Evidence of chronic ischaemia in the rest of the foot clinches the diagnosis
neuropathy, trauma, and changes in the bone metabolism.
(Table 26.4 for differences between arterial and venous ulcers).
Treatment
Immobilisation of the foot in a plaster of Paris
NEUROGENIC ULCER, NEUROPATHIC ULCER,
TROPHIC ULCER (Figs 26.14 and 26.15)
posterior slab with a walking boot almost cures the ulcer within 2–3 weeks, provided the primary disease (e.g. leprosy) is also controlled. If the ulcer is non-
This type of ulcer develops in an anaesthetic limb,
which may be caused by:
– Diabetic neuropathy – Meningomyelocele – Leprosy
healing with slough, initial management should include de-sloughing agents and surgical removal of the slough. Limb which does not serve any purpose for walking necessitates amputation as in advanced cases of Charcot’s foot.
Section II General Surgery
Figs 26.14 and 26.15: Neuropathic ulcer—classical site over the heel
Differential Diagnosis of Leg Ulcer and Pressure Sore
163
TROPICAL ULCER
It occurs in tropical countries. The precipitating factors are:
Malnutrition
Humid zones
Poor immunity
Trauma or insect bite
The infection is caused by Vincent’s organisms like
bacteroides, B. fusiformis, and Borrelia vincentii. It starts as a pustule with extensive inflammation. The pustule bursts and the ulcer spreads rapidly and causes destruc­tion of the surrounding tissue. Hence, it is also known
1
as a phagedenic ulcer.
The edges are undermined, the floor contains slough, and there copious seropurulent discharge is present. Healing is delayed for up to a month. Metronidazole may be useful in bringing down the inflammation. Broad-spectrum antibiotics may also be required in cases of secondary infections. If healing takes place, it leaves behind a scar.
POST-THROMBOTIC ULCER
It occurs due to deep vein thrombosis. It may affect calf veins or may be due to femoral vein thrombosis. It is an example of a venous ulcer or a gravitational ulcer.
Precipitating Factors
Accidents involving the lower leg
Childbirth
Abdominal operation.
Clinical Features
Bursting pain in the limb
Extensive induration of the leg or thigh depending
on site of thrombosis
Nonhealing with scanty granulation tissue
Deep—always infiltrates the deep fascia
Due to increased hydrostatic venous pressure, the
part is significantly indurated (cyanotic induration), pigmented, and thickened with a rise in local temperature.
The ulcer is not associated with superficial varico-
sity.
Homan’s sign: It is positive in calf vein thrombosis
(pain in the calf region on forcible dorsiflexion of the foot with the knee extended).
Moses’ sign: Squeezing of the calf muscles from side
to side produces pain. These two signs are positive in acute cases.
Treatment
Rest and elevation of the leg
Appropriate antibiotics
Elastic crepe bandage
With conservative treatment for a few days to a few
weeks, veins may recanalise and the ulcer may heal. The treatment is often very difficult (Chapter 30 on varicose veins).
RARE ULCERS
2
MARTORELL’S ULCER
Affects elderly patients over the age of 50 years.
Commonly affects hypertensive patients (hence, the
name hypertensive ulcer).
Atherosclerosis is also a precipitating factor, even
though peripheral pulses are usually present.
It occurs due to sudden obliteration of end-arterioles
of the skin on the back or lateral side of the calf region.
Severe pain
Ischaemic patch of skin which develops into a deep,
punched out, nonhealing ulcer.
Delayed healing due to vascular insufficiency.
BAZIN’S ULCER
Exclusively occurs in young females in the lower
third of the leg and ankle region.
Usually seen in obese patients who have thick ankles
and an abnormal amount of subcutaneous fat.
It begins with reddish-purplish nodules (hence, the
name erythrocyanosis frigida) on the calves, which later rupture and produce a nonhealing ulcer.
The aetiology of these ulcers is unclear. It may be
due to ischaemia of the lower leg due to spasm of branches of the posterior tibial and peroneal arteries. These vessels are abnormally sensitive to hot and cold weather, similar to Raynaud’s disease. In some cases, tubercular bacilli have been isolated, with ulcers responding to antitubercular treatment.
These ulcers are managed conservatively.
Sympathectomy may be beneficial in those patients
who are hypersensitive to weather changes.
1
Phagedenic (to eat). Rapidly spreading, ulcerative, destructive lesion. It can occur in the oral cavity and also over the penis.
2
Students should not offer these ulcers as clinical diagnosis. They are rare ulcers, with rare clinical interest.
Section II General Surgery